Thus, in our experimental conditions, GM-CSF, together with other cytokines usually associated with RA pathogenesis, but with capacities to attract lymphocytes with distinct phenotypes, like MIP-1α, MIP-1β, 6CKine, and RANTES, could be modulating specific T-cell functions in favour of a wider host defence. The gene discussed is CCL4; the disease is rheumatoid arthritis.